The objective of this study is to determine whether prostaglandins (PG) are released from the myocardium of the cat after coronary artery occlusion and whether they interact with the cardiac sympathetic innervation to produce an arrhythmogenic or antiarrhythmic effect. We intend to explore whether certain PG promote ventricular arrhythmia and ventricular fibrillation (VF) after occlusion by acting on the sympathetic nervous system while other PG prevent arrhythmia by suppressing sympathetic activity. We will determine quantitative and qualitative release of PG from the ischemic and non-ischemic myocardium by sampling blood from the great cardiac vein and comparing it with blood samples from the coronary sinus at various times after abrupt occlusion of the left anterior descending coronary artery (LAD) in cats anesthetized with alpha-chloralose. Cardiac sympathetic activity will be assessed by measuring plasma norepinephrine levels in the same blood samples. The degree of ischemia will be evaluated by measuring myocardial CPK-MB release in these blood samples while the extent of infarction will be determined 5 hours after LAD occlusion using macroscopic dehydrogenase staining. The release of PG and norepinephrine will be correlated with the severity of ventricular arrhythmia and the incidence of VF. These studies will be conducted against different backgrounds of endogenous PG activity by employing the PG synthesis inhibitors indomethacin and sulfinpyrazone. Sympathetic influences will be removed by employing 6-Hydroxydopamine. This study should more clearly define the importance of PG activity in the genesis and severity of ventricular arrhythmia following coronary artery occlusion. The results of our study may provide newer therapeutic approaches to this life threatening event.